Myasthenia gravis is a remitting and relaxing neuromuscular disease of man characterized by muscle fatiguability which increases with exertion and improves with rest. Although the etiology and pathogenesis of myasthenia gravis are incompletely understood, extensive studies of the acethylcholine receptor and the immune system in the last three years have clarified many features of this disorder. Of interest to the present application is the observation that myastenic sera or myasthenic IgG results in accelerated disappearance of acetylcholine. The objective of the present research is to study this phenomenon in greater depth in an attempt to answer the following questions: 1. Is the accelerated degradation specific for myasthenic globulins, and is the reaction specific for the acetylcholine receptor? 2. Does the accelerated disappearance of receptor depend upon complete immunoglobulin molecule, or will fragments cause the same effect? 3. Is the process specific for the degradative phase, or does myasthenic globulin influence the rate of synthesis and insertion of acetylcholine receptor into surface membrane? 4. Does myasthenic globulin influence the turnover of acetylcholine receptor in innervated cells as it appears to do in non-innervated muscle cells?